The tetrahydrofuran-type abasic site analog (THF) induces large deletion mutations in human cells. To compare the large deletions induced by THF on leading and lagging strand templates, plasmid DNAs bearing the analog at a specific position outside the supF gene were introduced into human U2OS cells. The replicated DNAs recovered from the transfected cells were electroporated into an Escherichia coli indicator strain. THF on the lagging strand template produced more supF mutants than THF on the leading strand template. This unequal mutagenicity was due to the higher frequencies of not only large deletions but also untargeted base substitutions induced in the gene. These results suggested that both types of mutations occur more frequently when abasic sites are formed on the lagging strand template.

中文翻译：

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无碱基位点类似物在人细胞的前导链和滞后链模板上诱导的大缺失和非靶向取代。

四氢呋喃型无碱基位点类似物（THF）诱导人类细胞中的大型缺失突变。为了比较在前导链和滞后链模板上由THF诱导的大缺失，将在supF基因外部特定位置带有类似物的质粒DNA引入人U2OS细胞。从转染的细胞中回收的复制的DNA被电穿孔到大肠杆菌指示菌株中。滞后链模板上的THF比前链模板上的THF产生更多的supF突变体。这种不平等的诱变性是由于基因中诱导的不仅大缺失的频率较高，而且是非靶向碱基取代的频率较高。这些结果表明，当在落后链模板上形成无碱基位点时，两种类型的突变都更频繁地发生。